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Identification of patients at risk of thromboembolism poses a daunting problem. Nevertheless the availability of measurable plasma or serum factors may help to identify those patients at particular risk of thrombogenesis and whom may benefit from prophylactic anticoagulant therapy. My thesis investigates the roles of fibrinogen, fibrin turnover, endothelial dysfunction and lipoprotein(a) in thrombogenesis associated with two cardiovascular conditions at high thromboembolic risk, that is, atrial fibrillation and left ventricular dysfunction. Atrial fibrillation was found to be a common cardiac arrhythmia in a survey of emergency admissions over a six month period to my hospital. Heart failure and cerebrovascular events were the commonest presenting features, accounting for about half of all emergency admissions who were found to be in atrial fibrillation. This survey gave a comprehensive profile of how patients with atrial fibrillation were investigated and managed in a district general hospital. For example, a suboptimal application of standard investigations In patients with atrial fibrillation was identified together with a reluctance to perform cardioversion or to commence anticoagulant therapy. This being despite the increasingly important roles for these two therapeutic manoeuvres in the current management of atrial fibrillation. One possible reason for the low rate of introducing anticoagulation may be the uncertainty of many physicians in identifying patients at high thromboembolic risk. The availability of a suitable plasma marker of thrombogenesis may assist decision-making in these patients. Factors such as fibrinogen, von Willebrand factor and lipoprotein (a) have been associated with thrombosis, embolism and stroke. In addition, the fibrin D-dimer fragment is a marker of fibrin turnover and is indirectly a measure of intravascular thrombus fonnation. In my study, I have identified abnormalities of these plasma markers suggesting a prothrombotic state in patients with atrial fibrillation and left ventricular aneurysms. Patients with chronic atrial fibrillation, for example, have significant elevations of plasma fibrinogen and von Willebrand factor when compared to normal population values; and this is irrespective of aspirin or warfarin therapy. Those who are on no antithrombotic therapy have the highest levels of plasma fibrin D-dimer, suggesting the highest levels of intravascular fibrin turnover in these patients. In contrast, patients whom are established on warfarin have the lowest fibrin D-dimer levels, consistent with the beneficial effect of warfarin in reducing thrombogenesis. No significant effect on these factors with respect to atrial size, ventricular function (as measured by echocardiography), or underlying valve or ischaemic heart disease was noted. Cardioversion of atrial fibrillation to sinus rhythm replaces the irregular atrial activity of atrial fibrillation with the regular atrial systole of sinus rhythm. If thrombogenesis has a simple mechanical basis, cardioversion of atrial fibrillation should be expected to immediately normalise plasma fibrinogen and fibrin D-dimer levels. This does not appear to be the case, as in patients without warfarin therapy, plasma fibrin D-dimer falls sequentially over two weeks following cardioversion. This is partly due to the clearance of D-dimer from the circulation and that atrial systole may not resume immediately. In addition, there is little change in plasma fibrinogen levels, which may inpart be due to the individual variation in the return of atrial systole. Although clinical studies suggest a 'high risk' period for thromboembolism following cardioversion, no significant peak in plasma fibrinogen or fibrin D-dimer has been noted. This is In keeping with the hypothesis that any emboli are due to pre-formed thrombus rather than formation of new thrombus following cardioversion. Patients who are anticoagulated pre- and post-cardioversion have low plasma D-dimer levels, which do not alter over the two weeks' follow-up, consistent with the prophylactic effects of warfarin in reducing thromboembolic risks during cardioversion. If fibrin D-dimer is a suitable indicator of intravascular thrombogenesis, further evidence may be obtained by a study of patients with paroxysmal atrial fibrillation. These patients are regarded as at intermediate thromboembolic risk when compared to chronic atrial fibrillation and those in sinus rhythm. Patients with paroxysmal atrial fibrillation (on no warfarin therapy) indeed do have intermediate levels of plasma fibrinogen and fibrin D-dimer, in keeping with clinical observations. This suggests that flow abnormalities may be important in thrombogenesis, as sustained irregular atrial activity (in chronic atrial fibrillation) causes greater abnormalities in markers of thrombogenesis when compared to patients with intermittent irregular atrial contractions (for example, paroxysmal atrial fibrillation) and those with normal, regular atrial systolic function (in sinus rhythm).